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This is possibly due to the conversion of erythrocytic GSH into GSSG, in line with previous reports

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Pyridoxal isonicotinoyl hydrazone is mentioned here because of its ability to permeate the mitochondrion and remove excess iron in vitro in a cellular model [520], or in vivo in the muscle creatine kinase frataxin knockout mouse model of Friedreich's ataxia that suffers mitochondrial iron-loading of the heart [521]
